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Heat shock induces HIV-1 replication in chronically infected promyelocyte cell line OM10.1

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Summary

A long period of clinical latency before development of symptoms is characteristic of human immunodeficiency virus type 1 (HIV-1) infection. OM10.1, a promyelocyte cell line latently infected with HIV-1, has been developed as a model for studying the mechanism of viral latency and the activation of virus expression. We found that this latently infected cell line with heat shock at 42°C for 2 h resulted in a high level of HIV-1 production without addition of any cytokines. The mechanism of activation was analyzed by using anti-TNF-α antibody and various inhibitors. Although the TNF-α level in culture supernatants was below the sensitivity of an ELISA assay system, addition of anti-TNF-α antibody in culture medium could partially suppress the heat shock induced HIV-1 production. Staurosporine (PKC inhibitor), pentoxifylline (NF-ϰB inhibitor), and Ro5-3335 (HIV-1 Tat inhibitor) also inhibited significantly the heat shock induced virus activation. In particular, staurosporine achieved approximately 90% inhibition of the HIV-1 antigen expression in heat shock-treated OM10.1 at a non-toxic concentration. Although the mechanism of HIV-1 activation with heat shock has not been fully elucidated yet, it is presumed PKC plays an important role in HIV-1 activation. Thus, the present observations will provide a further insight into the pathogenesis of HIV-1 infections.

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Authors and Affiliations

  1. Department of Microbiology, Fukushima Medical College, Fukushima, Japan

    K. Hashimoto, M. Sato & S. Shigeta

  2. Division of Human Retroviruses, Center for Chronic Viral Diseases, Faculty of Medicine, Kagoshima University, Kagoshima, Japan

    M. Baba

  3. Roku-chome Clinic, Sendai, Japan

    K. Gohnai

Authors
  1. K. Hashimoto
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  2. M. Baba
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  3. K. Gohnai
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  4. M. Sato
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  5. S. Shigeta
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Hashimoto, K., Baba, M., Gohnai, K. et al. Heat shock induces HIV-1 replication in chronically infected promyelocyte cell line OM10.1. Archives of Virology 141, 439–447 (1996). https://doi.org/10.1007/BF01718308

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  • DOI: https://doi.org/10.1007/BF01718308

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